[7] The complex of XPC-RAD23B is the initial damage recognition factor in global genomic nucleotide excision repair (GG-NER).

XPC-RAD23B recognizes a wide variety of lesions that thermodynamically destabilize DNA duplexes, including UV-induced photoproducts (cyclopyrimidine dimers and 6-4 photoproducts ), adducts formed by environmental mutagens such as benzo[a]pyrene or various aromatic amines, certain oxidative endogenous lesions such as cyclopurines and adducts formed by cancer chemotherapeutic drugs such as cisplatin.

[8] Although most studies have been performed with XPC-RAD23B, it is part of a trimeric complex with centrin-2, a calcium-binding protein of the calmodulin family.

[8] The protein expression level of RAD23B can be epigenetically repressed, either by promoter methylation of the RAD23B gene[9][10] or by either of two microRNAs (miR-744-3p[11] or miR-373[12]).

[9] and reduced by promoter methylation in a small proportion of non-small cell lung cancer (NSCLC) tumours.